• Shuzhuo Zhang, Xu Jin, Zerong You, Shuxing Wang, Grewo Lim, Jinsheng Yang, Michael McCabe, Na Li, John Marota, Lucy Chen, and Jianren Mao.
• MGH Center for Translational Pain Research, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA Department of Anesthesia and Pain Therapy, Beijing Tiantan Hospital Affiliated to Capital Medical University, Beijing 100050, China.
• Pain. 2014 Aug 1; 155 (8): 1504-1515.

AbstractAnxiety disorder is a comorbid condition of chronic pain. Analgesics and anxiolytics, subject to addiction and abuse, are currently used to manage pain and anxiety symptoms. However, the cellular mechanism underlying chronic pain and anxiety interaction remains to be elucidated. We report that persistent nociception following peripheral nerve injury induced anxiety-like behavior in rodents. Brain expression and release of neuropeptide S (NPS), a proposed endogenous anxiolytic peptide, was diminished in rodents with coexisting nociceptive and anxiety-like behaviors. Intracerebroventricular administration of exogenous NPS concurrently improved both nociceptive and anxiety-like behaviors. At the cellular level, NPS enhanced intra-amygdaloidal inhibitory transmission by increasing presynaptic gamma-aminobutyric acid (GABA) release from interneurons. These findings indicate that the interaction between nociceptive and anxiety-like behaviors in rodents may be regulated by the altered NPS-mediated intra-amygdaloidal GABAergic inhibition. The data suggest that enhancing the brain NPS function may be a new strategy to manage comorbid pain and anxiety. Copyright © 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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